Tony Goldstone attended medical school at both Cambridge and Oxford Universities, and trained in general medicine, adult endocrinology and diabetes at the Hammersmith, St. Bartholomew’s and Royal London Hospitals in London. He obtained his Ph.D. from Imperial College London on the hypothalamic control of feeding and metabolism.
He has researched and published widely on hormonal control of appetite, neuroendocrine, hypothalamic and metabolic abnormalities in obesity and the genetic Prader-Willi syndrome, particularly investigating the causes of hyperphagia, through pre-clinical, clinical, post-mortem, genetic, interventional, fat and brain imaging studies. This includes work as a research fellow at the Netherlands Institute for Brain Research in Amsterdam and the Division of Pediatric Genetics at the University of Florida, USA.
He was a Senior Clinician Scientist in the Metabolic and Molecular Imaging Group, MRC Clinical Sciences Centre, Imperial College London until 2014, and is now based in the Neuropsychopharmacology Unit, Centre for Psychiatry, and Computational, Cognitive and Clinical Neuroimaging Laboratory in the Division of Brain Sciences, at Hammersmith Hospital where he leads the PsychoNeuroEndocrinology Research Group investigating the neurobiology of the body-brain axis in modifying eating and addictive behaviours in obesity, and smoking and alcohol dependence
His research programme uses comprehensive phenotyping in humans including functional and structural neuroimaging using MRI, cognitive and psychological testing, assessment of gut and pituitary hormones, metabolism, appetite and eating behaviour, to examine body-brain interactions in the regulation of food hedonics, preference and reward processing, and addictive behaviours (such as impulsivity, compulsivity, emotional reactivity and stress sensitivity) in obesity, and the influence of dietary, hormonal, pharmacological and bariatric surgical interventions, and genetic variants.
His research themes include investigating the underlying mechanisms to aid development of novel therapies of:
(i) Changes in food reward, and eating and addictive behaviours after bariatric surgery and other interventions for obesity, including gastric bypass surgery and the duodenal-jejunal endoluminal bypass liner
(ii) Links between nutritional state, gut hormones, and addictive behaviours as potential treatments for smoking and alcohol dependence, and other addictions
(iii) Pathophysiology of the genetic obesity Prader-Willi syndrome including gastrointestinal hormone abnormalities
(iv) Novel genetic causes of syndromic obesity including carboxypeptidase E mutations and use of next generation sequencing
v) Hormonal and metabolic influences on brain recovery after traumatic brain injury
He has been a Consultant Endocrinologist at Imperial College Healthcare NHS Trust since 2005 based at the Hammersmith Hospital and St. Mary's Hospital.
He runs specialist adult clinics for patients with Prader-Willi syndrome and genetic obesity, and endocrine dysfunction after traumatic brain injury (in a multi-disciplinary clinic with Neurology and Psychiatry), as well as in-patient work in Acute Medicine.
His public engagement work includes talks such as ‘Guts or Brain? Where hormones regulate appetite’, Food, Glorious Food! British Neuroscience Association Christmas Symposium 2011 at The Royal Society, London; ‘Obesity: what lies in weight?’, Edinburgh Science Festival 2013; ‘Separating the Fat from the Fiction: Food choices’, Edinburgh Science Festival 2014. His research has featured in several TV programs including BBC1 ‘10 Things You Need to Know about Losing Weight’, Channel 4 ‘Embarrassing Fat Bodies’, BBC Horizon ‘The Truth about Fat’, BBC2 ‘The Men Who Made us Fat’, and BBC Scotland ‘Addicted to Pleasure’, and in the BBC Science video ‘What is fat?’.
et al., 2016, Increased colonic propionate reduces anticipatory reward responses in the human striatum to high-energy foods, American Journal of Clinical Nutrition, Vol:104, ISSN:0002-9165, Pages:5-14
et al., 2016, Prevalence and correlates of vitamin D deficiency in adults after traumatic brain injury, Clinical Endocrinology, Vol:85, ISSN:0300-0664, Pages:636-644
et al., 2016, Link Between Increased Satiety Gut Hormones and Reduced Food Reward After Gastric Bypass Surgery for Obesity, Journal of Clinical Endocrinology & Metabolism, Vol:101, ISSN:0021-972X, Pages:599-609
et al., 2014, Obese patients after gastric bypass surgery have lower brain-hedonic responses to food than after gastric banding, Gut, Vol:63, ISSN:0017-5749, Pages:891-902
et al., 2014, Ghrelin mimics fasting to enhance human hedonic, orbitofrontal cortex, and hippocampal responses to food, American Journal of Clinical Nutrition, Vol:99, ISSN:0002-9165, Pages:1319-1330
et al., 2014, Hyperphagia: Current Concepts and Future Directions Proceedings of the 2nd International Conference on Hyperphagia, Obesity, Vol:22, ISSN:1930-7381, Pages:S1-S17
et al., 2013, Pituitary Dysfunction after Blast Traumatic Brain Injury: The UK BIOSAP Study, Annals of Neurology, Vol:74, ISSN:0364-5134, Pages:527-536
et al., 2013, Loss-of-function mutations in SIM1 contribute to obesity and Prader-Willi-like features, Journal of Clinical Investigation, Vol:123, ISSN:0021-9738, Pages:3037-3041
et al., 2012, Gastric bypass surgery for obesity decreases the reward value of a sweet-fat stimulus as assessed in a progressive ratio task, American Journal of Clinical Nutrition, Vol:96, ISSN:0002-9165, Pages:467-473
et al., 2012, The Missing Risk: MRI and MRS Phenotyping of Abdominal Adiposity and Ectopic Fat, Obesity, Vol:20, ISSN:1930-7381, Pages:76-87
et al., 2009, Fasting biases brain reward systems towards high-calorie foods, European Journal of Neuroscience, Vol:30, ISSN:0953-816X, Pages:1625-1635
et al., 2008, Recommendations for the Diagnosis and Management of Prader-Willi Syndrome, Journal of Clinical Endocrinology & Metabolism, Vol:93, ISSN:0021-972X, Pages:4183-4197
Goldstone AP, Beales PL, 2008, Genetic obesity syndromes, Frontiers of Hormone Research, Vol:36, ISSN:0301-3073, Pages:37-60
et al., 2005, Fasting and postprandial hyperghrelinemia in Prader-Willi syndrome is partially explained by hypoinsulinemia, and is not due to peptide YY3-36 deficiency or seen in hypothalamic obesity due to craniopharyngioma, Journal of Clinical Endocrinology & Metabolism, Vol:90, ISSN:0021-972X, Pages:2681-2690
et al., 2004, Somatostatin infusion lowers plasma ghrelin withoug reducing appetite in adults with Pradi-Willi syndrome, Journal of Clinical Endocrinology & Metabolism, Vol:89, ISSN:0021-972X, Pages:4162-4165
Goldstone AP, 2004, Prader-Willi syndrome: advances in genetics, pathophysiology and treatment, Trends in Endocrinology and Metabolism, Vol:15, ISSN:1043-2760, Pages:12-20
Goldstone AP, Unmehopa UA, Swaab DF, 2003, Hypothalamic growth hormone-releasing hormone (GHRH) cell number is increased in human illness, but is not reduced in Prader-Willi syndrome or obesity, Clinical Endocrinology, Vol:58, ISSN:0300-0664, Pages:743-755
et al., 2001, Visceral adipose tissue and metabolic complications of obesity are reduced in Prader-Willi syndrome female adults: Evidence for novel influences on body fat distribution, Journal of Clinical Endocrinology & Metabolism, Vol:86, ISSN:0021-972X, Pages:4330-4338